In the future the following studies will be conducted: 1) The relationship between metabolic, histological and external signs of deficiency in rapidly induced vitamin A deficiency. Changes in steady state metabolite and amino acid levels will be correlated with signs of vitamin A deficiency. Labeled compounds will be employed to monitor the fate of compounds (such as threonine) which are markedly depressed following the onset of deficiency. 2) Abnormal metabolites associated with vitamin A deficiency. Abnormal compounds associated with the onset of deficiency will be identified and quantitated. The possibility of a clinical test for vitamin A deficiency will be investigated. 3) Receptor sites for RBP-vitamin A complex and vitamin A. Preformed RBP-11, 123H retinol complex will be injected into deficient rats and the fate of the label determined. 4) Vitamin A status and mucopolysaccharide synthesis. Immuno-fluorescent studies and H-3-thymidine pulse labeling of goblet cells will be conducted to better determine whether vitamin A affects glycoprotein synthesis directly, or the differentiation and migration of goblet cells. 5) Immune responses in vitamin A deficiency: Local and systemic immune responses will be studied, with emphasis on the possible role of secretary IgA, and association constants of serum antibodies.